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Biomedical subjects

J F Butterworth

Publications and source records attributed to J F Butterworth.

At least 19 recordsLinked to original sources
PubMed1992

Parathyroid hormone responses to marked hypocalcemia in infants and young children undergoing repair of congenital heart disease.

OBJECTIVES: The integrity of the parathyroid axis was tested in 18 infants and young children undergoing repair of congenital heart disease with cardiopulmonary bypass. BACKGROUND: Infants are believed to have an immature parathyroid hormone response to hypocalcemia. Whereas adults are known to respond appropriately to hypocalcemia during cardiopulmonary bypass, children have not been studied carefully. METHODS: Calcium, magnesium, parathyroid hormone, phosphate and total protein were measured in blood samples withdrawn at defined times before, during and after cardiopulmonary bypass. RESULTS: At the initiation of cardiopulmonary bypass, ionized calcium decreased markedly in 12 infants less than or equal to 24 months old (mean +/- SEM 1.11 +/- 0.04 to 0.29 +/- 0.05 mM) and decreased significantly in 6 young children greater than 24 months old (1.19 +/- 0.02 to 0.42 +/- 0.12 mM). In response to hypocalcemia, parathyroid hormone concentration increased significantly in both the infants (from 42 +/- 8 to 103 +/- 29 and 85 +/- 22 pg/ml) and the young children (from 39 +/- 8 to 44 +/- 20 and 92 +/- 30 pg/ml). Before separation from cardiopulmonary bypass, increased parathyroid hormone concentration restored ionized calcium concentration to 0.75 +/- 0.03 mM in the infants and to 0.92 +/- 0.07 mM in the young children. There was no significant influence of either age or the use of deep hypothermia and circulatory arrest on either calcium or parathyroid hormone responses. Total magnesium and total protein concentrations decreased on initiation of cardiopulmonary bypass and thereafter remained stable. Phosphate concentrations were unchanged during the study. CONCLUSIONS: In infants and young children undergoing cardiac surgery, the parathyroid hormone response to both hypocalcemia and to rising ionized calcium concentrations was at least as great as that of adults. Thus, the calcium-parathyroid-vitamin D axis functions in infants and young children as it does in adults.

Blood Proteins↗
PubMed1992

Is calcium or ephedrine superior to placebo for emergence from cardiopulmonary bypass?

To determine whether ephedrine or CaCl2 improves hemodynamics in cardiac surgery patients emerging from cardiopulmonary bypass, three sequential doses of either CaCl2 (200 mg/dose; n = 12), ephedrine (5 mg/dose; n = 12), or placebo (n = 12) were administered in a prospective, randomized, double-blind fashion. Thermodilution volumetric catheters were used to calculate right ventricular (RV) volumes and ejection fraction. The first dose of ephedrine improved RV stroke volume from 57 +/- 3 to 63 +/- 4 mL/beat (P < 0.05) and ejection fraction from 44 +/- 2% to 49 +/- 2% (P < 0.05). Subsequent doses maintained this improvement but without further change. In contrast, placebo and CaCl2 had minimal effects on RV end-systolic volume, stroke volume, and ejection fraction. After the third injection of ephedrine, mean arterial pressure had significantly increased from 78 +/- 2 to 93 +/- 4 mmHg (P < 0.05) in contrast to insignificant increments with placebo and CaCl2. Serum ionized calcium increased by 6% to 8% after each CaCl2 bolus but remained stable in the ephedrine and placebo groups. CaCl2 failed to improve RV performance in mildly hypocalcemic patients during separation from cardiopulmonary bypass. In patients with normal preoperative ventricular function, ephedrine more effectively improved RV performance and arterial blood pressure than placebo or CaCl2, and is a suitable short-acting drug to assist separation from cardiopulmonary bypass.

Adult↗
PubMed1992

Dobutamine increases heart rate more than epinephrine in patients recovering from aortocoronary bypass surgery.

To determine whether epinephrine might prove to be a cost-effective substitute for dobutamine, two 8-minute infusions of either epinephrine (10 and 30 ng/kg/min, n = 28) or dobutamine (2.5 and 5 micrograms/kg/min, n = 24) were administered to 52 patients recovering in the intensive care unit (ICU) after aortocoronary bypass (CABG) surgery. At the higher dose, both drugs significantly (P < .05) increased cardiac index (CI), epinephrine from 2.8 +/- 0.1 at baseline to 3.3 +/- 0.1 L/min/m2, and dobutamine from 3.2 +/- 0.1 at baseline to 4.1 +/- 0.2 L/min/m2. Epinephrine increased CI significantly less than dobutamine. Both drugs significantly increased stroke volume index (SVI), epinephrine from 32 +/- 1 at baseline to 36 +/- 1 mL/beat/m2, and dobutamine from 36 +/- 1 at baseline to 40 +/- 2 mL/beat/m2. At the higher dose, the effects of the two drugs on SVI were indistinguishable. On the other hand, while the higher dose of both drugs significantly increased heart rate (HR), epinephrine from 88 +/- 2 at baseline to 90 +/- 2 beats/min and dobutamine from 89 +/- 2 at baseline to 105 +/- 3 beats/min, the increase following the higher dose of dobutamine was significantly greater than that seen after epinephrine. Effects of the two drugs on mean arterial pressure, central venous pressure, pulmonary artery occlusion pressure, systemic vascular resistance, pulmonary vascular resistance, and left-ventricular stroke work did not significantly differ. Similar results were obtained in the subset of patients with baseline CI less than 3 L/min/m2 who more closely resembled patients who might acutely require inotropic drug administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1992

A randomized, blinded, placebo-controlled evaluation of calcium chloride and epinephrine for inotropic support after emergence from cardiopulmonary bypass.

Forty hemodynamically stable patients were randomized to receive an intravenous bolus of either calcium chloride (5 mg/kg) (n = 20) or placebo (n = 20) (phase I). Six minutes later, they received either an epinephrine (30 ng.kg-1.min-1) (n = 20) or placebo (n = 20) infusion (phase II). Hemodynamic and ionized calcium measurements were obtained in phase I at baseline and at 3 and 6 min after the bolus, and in phase II, at 3 and 6 min (study times 9 and 12 min) after initiation of the infusion. Compared with placebo, calcium did not significantly increase cardiac index but significantly increased mean arterial pressure. Calcium improved cardiac index from 2.46 +/- 0.12 (mean +/- SEM) to 2.74 +/- 0.12 L.min-1.m-2; likewise, placebo improved cardiac index from 2.51 +/- 0.15 to 2.74 +/- 0.15 L.min-1.m-2. Mean arterial blood pressure increased with calcium from 74 +/- 2 to 82 +/- 3 mm Hg compared with a placebo change of 74 +/- 2 to 76 +/- 2 mm Hg. Patients who received the epinephrine infusion (n = 20) demonstrated a significant increase in cardiac index at time 12 min compared with patients receiving only placebo (n = 20). Cardiac index of the epinephrine group increased from 2.56 +/- 0.15 to 2.92 +/- 0.22 L.min-1.m-2, whereas in the placebo group it decreased from 2.86 +/- 0.13 to 2.78 +/- 0.12 L.min-1.m-2. Prior administration of calcium did not alter the subsequent response to epinephrine (n = 10) compared with patients receiving epinephrine alone (n = 10). We conclude that cardiac index improves with time without drug therapy after bypass. Calcium chloride increases mean arterial blood pressure but not cardiac index immediately after cardiopulmonary bypass, whereas low-dose epinephrine significantly increases both cardiac index and mean arterial blood pressure without causing tachycardia in these patients. Calcium chloride (5 mg/kg) did not augment or inhibit the hemodynamic response to an epinephrine infusion.

Calcium↗
PubMed1992

Calcium inhibits the cardiac stimulating properties of dobutamine but not of amrinone.

To contrast the effect of increasing blood calcium concentrations on the cardiovascular actions of intravenous beta-adrenergic agonists and phosphodiesterase inhibitors, 46 patients recovering from aortocoronary bypass surgery received either dobutamine or amrinone both in the presence and absence of a calcium infusion. Cardiac output, systemic arterial pressure, pulmonary arterial pressure, central venous pressure, pulmonary artery occlusion pressure, heart rate, and blood ionized calcium concentration were measured before and during infusions of dobutamine (2.5 and 5.0 micrograms/kg/min) and amrinone (0.75 mg/kg bolus + 10 micrograms/kg/min or 2.25 mg/kg bolus + 20 micrograms/kg/min). After the initial dobutamine infusion period, patients were randomly and blindly assigned to receive either a calcium or placebo infusion, and the dobutamine infusions were repeated. Because of the long duration of amrinone's actions, the amrinone maintenance infusion was continued while randomized, blinded infusion of either calcium or placebo was added. Dobutamine (5 micrograms/kg/min) increased cardiac output from 7.1 +/- 0.3 L/min to 9.1 +/- 0.4 L/min, and increased heart rate from 93 +/- 4 beats/min to 107 +/- 4 beats/min. Systemic vascular resistance decreased and stroke volume increased. Dobutamine had no significant effects on other hemodynamic values. Amrinone (2.25 mg/kg bolus + 20 micrograms/kg/min) increased cardiac output from 5.6 +/- 0.4 L/min to 6.9 +/- 0.5 L/min, and increased heart rate from 87 +/- 3 beats/min to 98 +/- 3 beats/min. Amrinone decreased mean arterial pressure, systemic vascular resistance, pulmonary artery occlusion pressure, central venous pressure, and pulmonary artery pressure. Calcium infusion increased arterial pressure (8 to 13 percent) but had no significant effects on any other hemodynamic parameters. Calcium reduced the increase in cardiac output produced by dobutamine by 30 percent, but it did not alter the cardiotonic actions of amrinone. Thus, calcium inhibits the cardiotonic actions of certain beta-adrenergic agonists, most likely by interfering with signal transduction through the beta-adrenergic receptor complex.

Amrinone↗
PubMed1992

Do antiarrhythmic doses of magnesium potentiate vecuronium?

The purpose of this study was to investigate whether magnesium sulfate (MgSO4) at a dose commonly used to treat arrhythmias potentiates vecuronium. After Institutional Review Board approval, 20 randomly assigned, consenting patients received a bolus of either MgSO4 (30 mg/kg) or placebo in a blinded fashion. Immediately after receiving the bolus of either MgSO4 or placebo, the study patients were taken to the operating room (OR) and anesthetized. The ED95 of vecuronium was determined in both groups by administering 10 micrograms/kg boluses of vecuronium until 95% twitch depression was measured. Delay to 25% twitch height recovery (indicating that the neuromuscular block could be reversed for extubation) was measured in 10 patients. Ultrafilterable magnesium levels were measured in a total of 13 patients. Magnesium levels were drawn before the magnesium/placebo bolus, 5 minutes after bolus, and 30 minutes after bolus. The data did not demonstrate any relationship between the use of MgSO4 at 30 mg/kg doses and either the ED95 or the duration of vecuronium. A 30 mg/kg bolus of MgSO4 roughly doubled ultrafilterable magnesium levels from baseline. The limited sample size precluded making any firm conclusions from this data. The data trend suggested that antiarrhythmic doses of MgSO4 may not potentiate vecuronium.

Adolescent↗
PubMed1991

Magnesium inhibits the hypertensive but not the cardiotonic actions of low-dose epinephrine.

Intravenous magnesium supplementation is often used to control cardiac arrhythmias and coronary artery vasospasm resulting from disturbances of magnesium homeostasis after coronary artery bypass surgery. Many such patients also require inotropic drug support of depressed myocardial function. However, increased serum magnesium concentrations directly depress cardiac contractility in animals and may interfere with catecholamine actions. To determine whether small intravenous doses of magnesium sulfate (MgSO4) interfere with the cardiotonic actions of epinephrine, we examined the hemodynamic effects of MgSO4 and epinephrine infusion in 17 cardiac surgical patients on their 1st postoperative day in a prospective, controlled study. In 11 patients, infusion of MgSO4 (7-mg.kg-1 bolus followed by 10 mg.kg-1.h-1 as a continuous infusion) increased serum magnesium concentrations by 44% (mean +/- standard error of the mean [SEM] of 0.8 +/- 0.1 to 1.2 +/- 0.1 mM; P less than 0.01) but had no significant effect on heart rate; mean arterial, central venous, or pulmonary arterial occlusion pressures; or cardiac output. Epinephrine infusion (30 ng.kg-1.min-1) significantly increased cardiac index (2.7 +/- 0.1 to 3.1 +/- 0.21.min-1.m-2; P less than 0.05); this effect was not altered by MgSO4 administration (n = 11). However, MgSO4 significantly blunted epinephrine's hypertensive action and prevented a significant increase in mean arterial pressure during concurrent MgSO4-epinephrine administration. Six placebo control patients were given two sequential infusions of epinephrine separated by a placebo infusion to rule out an effect of time on the hemodynamic response to epinephrine. Mean arterial pressure and cardiac index responses to epinephrine were identical before and after placebo infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗
PubMed1991

Normal parathyroid hormone responses to hypocalcemia during cardiopulmonary bypass.

To determine whether the calcium-magnesium-parathyroid hormone-calcitriol (vitamin D) axis responds appropriately to the hypocalcemia that routinely follows initiation of cardiopulmonary bypass (CPB), we measured blood ionized calcium (CaI), total calcium (CaT), total magnesium (MgT), ultrafilterable magnesium (MgI), total protein, intact parathyroid hormone (PTH), and calcitriol concentrations at eight defined time points in 28 patients undergoing elective cardiac surgery. With the onset of CPB, CaI decreased from 1.14 +/- 0.02 to 0.91 +/- 0.03 mM, P less than 0.05) (n = 17), and then gradually returned to a normal value by the time of separation from CPB (0.98 +/- 0.01 mM). CaT, MgI, MgT, and total protein concentrations declined significantly upon initiation of CPB and remained depressed thereafter. PTH initially decreased upon initiation of CPB (from 50 +/- 8 to 24 +/- 9 pg/ml, n = 9, P less than 0.05), remained inappropriately decreased during the early phases of CPB, and then gradually increased to maximal concentrations in response to hypocalcemia (103 +/- 15 pg/ml) before emergence. Calcitriol concentrations (n = 8) were unchanged during surgery. Based on these initial results, which suggested an association between hypomagnesemia and the slow PTH response to hypocalcemia, measurements were repeated in 10 additional patients, to whom magnesium (Mg) (1 g MgSO4 in two separate intravenous doses) was administered. Mg administration neither altered the PTH response to ionized hypocalcemia nor hastened the return of CaI to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗
PubMed1991

Preoperative and intraoperative predictors of inotropic support and long-term outcome in patients having coronary artery bypass grafting.

The prognostic value of preoperative symptoms, preoperative left ventricular function, and intraoperative factors as related to postoperative outcome in coronary artery bypass grafting is unclear. This study was performed to identify risk factors that could be used as markers to predict immediate and long-term outcome, knowledge of which might allow physicians to modify these factors to decrease the likelihood of an adverse outcome. We retrospectively evaluated preoperative factors (including age, sex, New York Heart Association [NYHA] classification of symptoms, ejection fraction [EF], wall motion abnormalities, baseline left ventricular end-diastolic pressure [LVEDP], postradiographic contrast injection LVEDP, change in LVEDP with contrast injection, cardiac enlargement, and collateral vessels) and intraoperative factors (duration of bypass and aortic cross-clamp time) in 128 patients. The need for inotropic drug support was used as a marker of immediate outcome. A 36-mo follow-up used death and the postoperative NYHA classification of symptoms as markers of long-term outcome. The various factors associated with the use of inotropes and immediate outcome were analyzed by logistic regression. The factors related to inotrope use (and presumed adverse short-term outcome) in order of decreasing significance were lower EF, older age, cardiac enlargement, female sex, and higher baseline and postcontrast LVEDP. Patients with EF greater than or equal to 55%, but also having wall motion abnormalities and LVEDP change greater than or equal to 10 mm Hg, and all patients with EF less than 55% were more likely to require inotropic drug stimulation after cardiopulmonary bypass. Neither the change in LVEDP nor the presence of wall motion abnormalities independently predicted the need for postoperative inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

Effects of amrinone on cardiac index, venous oxygen saturation and venous admixture in patients recovering from cardiac surgery.

The hemodynamic and oxygen transport effects of low-dose (0.75 mg/kg loading dose + 10 micrograms/kg/min infusion, n = 12) and high-dose (2.25 mg/kg loading dose + 20 micrograms/kg/min infusion, n = 12) amrinone were evaluated in extubated patients 24 h after CABG. At both doses, amrinone significantly (p less than 0.05) increased HR, but decreased mean arterial, mean pulmonary artery, central venous and pulmonary artery occlusion pressures. High-dose amrinone significantly decreased systemic vascular resistance. Arterial oxygen saturation decreased significantly following both low- (97.8 +/- 0.4 to 95.6 +/- 0.9 percent) and high- (98.8 +/- 3.4 to 93.9 +/- 1.2 percent) dose amrinone. Pulmonary shunt increased significantly following low-dose amrinone and markedly increased Qs/Qt after high-dose amrinone. Although amrinone significantly increased cardiac index in a dose-dependent fashion (low:3.0 +/- 0.2 to 3.3 +/- 0.3 L/min/m2; high:2.7 +/- 0.2 to 3.4 +/- 0.2 L/min/m2), mixed venous oxygen saturation did not change. Thus, mixed venous oxygen saturation may not predict the hemodynamic response to amrinone infusion in postoperative surgical patients.

Amrinone↗
PubMed1990

Effect of adrenaline on plasma concentrations of bupivacaine following intra-articular injection of bupivacaine for knee arthroscopy.

We administered 0.5% bupivacaine 30 ml either with or without adrenaline 5 micrograms ml-1 randomly to 16 healthy outpatients, to determine the efficacy of local and intra-articular local anaesthesia for knee arthroscopy and whether or not adrenaline should be added to intra-articular bupivacaine. Bupivacaine concentrations were measured in plasma obtained 15, 30, 45 and 60 min after intra-articular injection. Patients receiving bupivacaine with adrenaline had significantly smaller plasma concentrations of bupivacaine at all times than did patients receiving plain bupivacaine. The maximal concentrations of bupivacaine in the plain group (median 515 ng ml-1, range 46-875 ng ml-1) were greater than those in the adrenaline group (median 33 ng ml-1, range 7-125 ng ml-1) (P = 0.001). All patients found the anaesthetic satisfactory. We conclude that intra-articular/local anaesthesia is satisfactory for outpatient arthroscopic surgery, and that adrenaline should probably be added to bupivacaine before intra-articular injection.

Adult↗
PubMed1990

Molecular mechanisms of local anesthesia: a review.

Impulse block by LA occurs through the inhibition of voltage-gated Na+ channels. Both protonated and neutral LAs can inhibit Na+ channels though interference with the conformational changes that underly the activation process (the sequence of events that occurs as channels progress from the closed resting state to the open conducting state). The occlusion of open channels contributes little to the overall inhibition. Local anesthetic inhibition of Na+ currents increases with repetitive depolarizations in a process called phasic block. Phasic block represents increased LA binding, either because more channels become accessible during depolarization or because the channel conformations favored by depolarization bind LA with higher affinity. The details of phasic block are dependent on LA chemistry: certain LAs bind and dissociate quite rapidly, others act more slowly; some LAs interact effectively with closed states that occur intermediately between resting and open states, others favor the open channel, and still others have a higher affinity for inactivated states. Channel activation accelerates LA binding, and LAs may bind more tightly to activated and inactivated than to resting channels. In this regard, both the modulated receptor and the guarded receptor hypotheses are valid. In binding to activated and inactivated channels, LAs prevent the conformational changes of activation and antagonize the binding of activator agents that poise channels in activated, open states. These reciprocal actions are one aspect of the concerted conformational rearrangements that occur throughout Na+ channels during gating. The LA binding site may exist in the channel's pore, at the membrane-protein interface, or within the protein subunits of the channel. Judging from its susceptibility to intracellular proteases and its accessibility to LAs with limited membrane permeability (i.e., quaternary LAs in the cytoplasm), the site lies nearer to the cytoplasmic than the external surface of the membrane. Nevertheless, protons in the external medium influence the dissociation of LA from the closed channel. Binding of LAs at the inhibitory site is weak and loose. If one accounts for the membrane-concentrating effects of LA hydrophobicity that are expressed as membrane: buffer partition coefficients equal to 10(2)-10(4), then the apparent LA affinities are low. The equilibrium dissociation constants calculated on the basis of free drug in the membrane are 1-10 mM, with a correspondingly weak binding to the inhibitory LA site. The stereospecificity of LA action is also relatively nonselective, suggesting a loose fit between ligand and binding site.(ABSTRACT TRUNCATED AT 400 WORDS)

Anesthesia, Epidural↗
PubMed1990

Pregnancy increases median nerve susceptibility to lidocaine.

To determine whether pregnancy renders women more sensitive to local anesthetics, nine nonpregnant and nine pregnant (third trimester) women underwent median nerve block at the wrist using 1% lidocaine HCl. Inhibition of median nerve A alpha sensory and motor fibers was assessed using measurements of sensory nerve action potential (SNAP) amplitude and compound motor action potential (CMAP) amplitude, respectively. Inhibition of median nerve C fibers was assessed by the increase in skin temperature and by the decrease in median (relative to ulnar) galvanic skin potential (GSP) amplitude. Lidocaine inhibited SNAP to a greater extent in pregnant than nonpregnant women at all time points (P = 0.019). CMAP declined differently in the pregnant and nonpregnant groups (P = 0.01): the pregnant subjects achieved steady state inhibition before the nonpregnant subjects. The two groups developed comparable steady state inhibition. Skin temperature was higher in pregnant women at all time points (P less than 0.0001); moreover, the increased skin temperature of pregnant women differed from that of the nonpregnant women (P = 0.037), reflecting a more rapid temperature increase in the pregnant women. GSP amplitude declined to 50% of control more rapidly in pregnant (mean = 4 min) than nonpregnant women (mean = 11.5 min), but these differences did not achieve statistical significance. It is concluded that pregnancy increases median nerve susceptibility to lidocaine.

Action Potentials↗
PubMed1990

Calcium does not augment phenylephrine's hypertensive effects.

Ca and phenylephrine, both of which increase mean arterial pressure (MAP), are often administered concurrently during resuscitation of critically ill patients. To determine whether the response to phenylephrine is potentiated by Ca administration, we studied eight adult patients 24 h after aortocoronary bypass surgery. Each patient received three doses of phenylephrine (150, 300, and 450 ng/kg.min), administered both with and without CaCl2 (5 mg/kg bolus followed by a 2-mg/kg.h infusion). Phenylephrine alone at 150, 300, and 450 ng/kg.min increased MAP by 2%, 6%, and 17%, respectively. Ca alone increased serum ionized Ca levels from 1.00 +/- .03 (SEM) to 1.20 +/- .02 mM (p less than .05) and increased MAP from 84 +/- 1 to 90 +/- 2 mm Hg (p less than .05), but had no effect on cardiac index (CI). When administered concurrently with Ca, phenylephrine at 150, 300, and 450 ng/kg.min increased MAP by 6%, 7%, and 13%, respectively. Phenylephrine had no effect on CI, pulmonary capillary wedge pressure, CVP, or heart rate whether or not it was administered with Ca. We conclude that concomitant Ca administration does not augment the hypertensive response to phenylephrine in normotensive patients recovering from open heart surgery.

Aged↗
PubMed1990

Calcium attenuates epinephrine's beta-adrenergic effects in postoperative heart surgery patients.

Epinephrine and calcium possess both cardiac inotropic and vasopressor activity. In addition, epinephrine's cardiovascular effects are mediated via increases in intracellular calcium. As a result, many clinicians administer the two agents together in an attempt to augment their effects. Although this approach seems rational, it has never been proven effective. We evaluated the cardiovascular and hyperglycemic actions of epinephrine (10 and 30 ng/kg/min), with and without calcium chloride administration (10 mg/kg bolus followed by 2 mg/kg/hr infusion), in a prospective, randomized, blinded, crossover designed study. Twelve adult patients were studied 1 day after aortocoronary bypass surgery. Calcium chloride raised ionized calcium levels from 1.06 +/- 0.03 (mean +/- SEM) to 1.44 +/- 0.05 mM (p less than 0.05). Calcium raised mean arterial pressure from 85 +/- 1 to 94 +/- 2 mm Hg (p less than 0.05) but had no significant effect on cardiac index. Epinephrine alone at 10 and 30 ng/kg/min significantly raised cardiac index from 2.7 +/- 0.2 to 3.0 +/- 0.2 (p less than 0.05) and 3.6 +/- 0.3 (p less than 0.05) l/min/m2. After calcium, epinephrine failed to significantly increase cardiac index. Epinephrine at 30 ng/kg/min significantly increased mean arterial pressure from 87 +/- 1 to 95 +/- 2 mm Hg (p less than 0.05). After calcium, epinephrine had no significant effect on blood pressure. In addition, epinephrine's hyperglycemic effect was blunted by calcium. Plasma epinephrine levels were similar during control and calcium infusions. We conclude that calcium blunts epinephrine's beta-adrenergic actions in postoperative cardiac surgery patients.

Blood Glucose↗
PubMed1990

Cooling potentiates lidocaine inhibition of median nerve sensory fibers.

To determine the effect of cooling on lidocaine potency, nine consenting volunteers underwent bilateral median nerve blocks using 1% lidocaine HCl solution. Room-temperature and ice-cold lidocaine were injected into either dominant or nondominant wrists. Subjects were blinded to the temperature of the anesthetic. Inhibition of A alpha sensory and motor fibers was assessed as the decline in sensory nerve action potentials and compound motor action potentials, respectively. Inhibition of C fibers was measured as an increase in skin temperature and a decline in galvanic skin potentials. All indices of nerve function demonstrated profound (P less than 0.001) time-related changes after injection of local anesthetic. When ice-cold lidocaine was injected, inhibition of sensory nerve action potentials was significantly greater at all time points (P = 0.001) than when room-temperature lidocaine was injected. Inhibition of C fibers as assessed by galvanic skin potentials was marginally faster (P = 0.07) when ice-cold lidocaine was used compared with room-temperature lidocaine. No differences between room-temperature and ice-cold lidocaine were observed in inhibition of compound motor action potentials, or in the increase in skin temperature. We conclude that inhibition of median sensory fibers may be increased by cooling 1% lidocaine HCl in an ice bath before injection.

Action Potentials↗
PubMed1990

Low concentrations of procaine and diethylaminoethanol reduce the excitability but not the action potential amplitude of hippocampal pyramidal cells.

To determine whether concentrations of diethylaminoethanol (DEAE) and procaine below those that reduce the amplitude of action potentials might alter the excitability of brain cells, a single microelectrode intracellular recording technique was used to measure firing threshold and action potential amplitude of pyramidal cells in rat hippocampal slices. At low concentrations of both DEAE (less than or equal to 5 mM) and procaine (less than or equal to 0.5 mM), firing threshold was significantly increased (P less than 0.01), whereas action potential spike amplitude was minimally altered. At higher concentrations, both drugs significantly decreased action potential spike amplitude (P less than 0.025) as well as increased firing threshold (P less than 0.001). Diethylaminoethanol tended to increase threshold relatively more than procaine, when drug concentrations that similarly reduced action potential amplitude were compared. All actions of DEAE and procaine were reversible. Inhibition of action potentials by DEAE and procaine was clearly concentration-dependent (P less than or equal to 0.015). Diethylaminoethanol effects on threshold were marginally concentration-dependent (P = 0.08); procaine did not demonstrate clear concentration-dependent effects (P = 0.33) over the concentrations tested in this study. These similar actions of procaine and DEAE on brain cells suggest a mechanism by which intravenous local anesthetics may contribute to the general anesthetic state. Moreover, it appears possible that procaine metabolism and DEAE accumulation may underlie the prolonged effects sometimes seen after intravenous procaine administration.

Action Potentials↗